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硫酸软骨素蛋白聚糖对早产儿脑白质损伤后轴突生长的抑制作用及其机制的研究进展

[Research advances in the inhibitory effect of chondroitin sulfate proteoglycans on axon growth after premature white matter injury and its underlying mechanisms].

作者信息

Tian Xiao-Jie, Gao Rui-Wei, Chen Chao

机构信息

Department of Neonatology, Children's Hospital of Fudan University/Key Laboratory of Neonatal Diseases of National Health Commission, Shanghai 201102, China com).

出版信息

Zhongguo Dang Dai Er Ke Za Zhi. 2025 Jul 15;27(7):875-880. doi: 10.7499/j.issn.1008-8830.2502018.

Abstract

White matter injury (WMI) is a major form of brain injury in preterm infants. Its characteristic pathological features primarily involve impaired development of oligodendrocyte precursor cells and structural damage to axons, which can lead to the neurological sequelae such as motor, behavioral, and cognitive dysfunctions. Chondroitin sulfate proteoglycans (CSPGs), as the important components of extracellular matrix, can participate in neuroinflammatory response mediated by microglial cells and dynamically balance glial scar reconstruction and axon growth by regulating specific receptors and signaling pathways. This article reviews the relationship between CSPGs and WMI, as well as the mechanisms by which CSPGs inhibit axon growth, focusing on the role of multi-target regulation of CSPGs in promoting axon plasticity and functional brain recovery, thereby providing a theoretical basis for improving the prognosis of preterm infants with WMI.

摘要

白质损伤(WMI)是早产儿脑损伤的主要形式。其特征性病理特征主要涉及少突胶质前体细胞发育受损和轴突结构损伤,这可导致运动、行为和认知功能障碍等神经后遗症。硫酸软骨素蛋白聚糖(CSPGs)作为细胞外基质的重要组成部分,可参与小胶质细胞介导的神经炎症反应,并通过调节特定受体和信号通路动态平衡胶质瘢痕重建和轴突生长。本文综述了CSPGs与WMI之间的关系,以及CSPGs抑制轴突生长的机制,重点关注CSPGs多靶点调节在促进轴突可塑性和脑功能恢复中的作用,从而为改善WMI早产儿的预后提供理论依据。

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